CVA

jeffreyasalonga,ptrp
Definition
• Cerebrovascular Accident (CVA)
- the sudden loss of neurological function caused by an interruption of
the blood flow to the brain (ischemic/hemorrhagic)
>24 hours

*Apoplexy- first term used to describe CVA; unconsciousness or

incapacity resulting from a cerebral hemorrhage
Temporal Classification
• Transient Ischemic Attack (TIA)
- refers to the temporary interruption of blood supply to the brain
- Symptoms of focal neurological deficit may last for only a few minutes
or for several hours, but by definition do not last longer than 24 hours
- After the attack is over there is no evidence of residual brain damage
or permanent neurological dysfunction
Temporal Classification
• TIA
- may result from a number of different etiological factors, including
occlusive episodes, emboli, reduced cerebral perfusion (arrhythmias,
decreased cardiac output, hypotension, overmedication with
antihypertensive medications, subclavian steal syndrome), or
cerebrovascular spasm
Temporal Classification
• TIA
- the major clinical significance of TIA is as a precursor to susceptibility
for both cerebral infarction and myocardial infarction. Approximately
15% of all strokes are preceded by a TIA, with the greatest risk of
occurrence within 90 days
Temporal Classification
• Reversible Ischemic Neurologic Deficit
- loss of neurologic fubction usually less than 3 weeks
- secondary to brain edema
Temporal Classification
• Deteriorating Stroke
- “stroke in evolution”
- usually secondary to thrombosis
Temporal Classification
• Stroke in the young
< 45 years old
secondary to hemorrhagic stroke
Risk Factors
• Non-modifiable Factors
a. Age- the incidence of stroke increases dramatically with age,
doubling in the decade after 65 years of age. Twenty-eight percent of
strokes occur in individuals younger than 65 years of age.
b. Gender- M>F; however, at the age of 85 years old, F>M
c. Race- African Americans
d. Family History
Risk Factors
• Modifiable Factors
a. Hypertension- most treatable
Risk Factors
• Modifiable Factors
b. Smoking- Current smokers have 2 to 4 times increased stroke risk
compared to nonsmokers or those who have quit for more than 10
year
c. Physical activity (moderate to vigorous exercise) is associated with
an overall 35% reduction in stroke risk whereas light exercise (walking)
does not appear to have the same benefit
d. Diet
Risk Factors
• Modifiable Factors
e. Obesity
Risk Factors
• Modifiable Factors
f. Hypercholesterolemia
Low density Lipoprotein- <100 mg/dL
Borderline: 130-159 mg/dL
High: 160-189 mg/dL
Very High: >190 mg/dL
Risk Factors
• Modifiable Factors
High Density Lipoprotein- >60 mg/dL
Male: <40 mg/dL
Female: <50 mg/dL
Etiology and Pathophysiology
• Atherosclerosis is a major contributory factor in cerebrovascular
disease
• It is characterized by plaque formation with an accumulation of lipids,
fibrin, complex carbohydrates, and calcium deposits on arterial walls
that leads to progressive narrowing of blood vessels
• Interruption of blood flow by atherosclerotic plaques occurs at
certain sites of predilection
Etiology and Pathophysiology
• For cells to survive, 20% to 25% of regular blood flow is required
• Ischemic Cascade- damaging cellular events
- the release of excess neurotransmitters (glutamate and aspartate)
produces a progressive disturbance of energy metabolism
- this results in an inability of brain cells to produce energy, particularly
adenosine triphosphate (ATP)
- this is followed by excess influx of calcium ions and pump failure of
the neuronal membrane
Etiology and Pathophysiology
• Excess calcium reacts with intracellular phospholipids to form free
radicals.
• Calcium influx also stimulates the release of nitric oxide and
cytokines. Both mechanisms further damage brain cells.
Etiologic Classification
I. Ischemic- 80-85%
- the result of a thrombus, embolism, or conditions that produce low
systemic perfusion pressures.
- resulting lack of cerebral blood flow (CBF) deprives the brain of
needed oxygen and glucose, disrupts cellular metabolism, and leads to
injury and death of tissues.
- A thrombus results from platelet adhesion and aggregation on
plaques
Etiologic Classification
• Thrombi lead to ischemia, or occlusion of an artery with resulting
cerebral infarction or tissue death (atherothrombotic brain infarction
[ABI])
• Thrombi can also become dislodged and travel to a more distal site in
the form of an intra-artery embolus. Cerebral embolus (CE) is
composed of bits of matter (blood clot, plaque) formed elsewhere
and released into the bloodstream, traveling to the cerebral arteries
where they lodge in a vessel, producing occlusion and infarction.
• The most common source of CE is disease of the cardiovascular
system
Etiologic Classification
I. Ischemic- 80-85%
A. Thrombosis
- large vessel thrombosis
- 40%- most common
- secondary to atherosclerosis
- onset: gradual
- Sites: MCA, VBA, Common Carotid
Etiologic Classification
B. Embolic
- 20-25%
- 2nd most common
- sources: Heart Embolism, Paradoxical Embolism
- onset: abrupt
Etiologic Classification
C. Small Vessel Thrombosis
- 15-20%
Etiologic Classification
II. Hemorrhagic - 15-20%
A. Intracerebral Hemorrhage/ ICH/IH
- caused by rupture of a cerebral vessel with subsequent bleeding into
the brain
- 15%
- also known as Hypertensive Hemmorrhage
- secondary to hypertension
Etiologic Classification
* Charcot- Bouchard Aneurysm
- also known as pseudoaneurysm
- secondary to longstanding hypertension
Sites:
Putamen
Subcortical white matter
Thalamus
Pons
Cerebellum
Etiologic Classification
B. Subarachnoid Hemorrhage/ SAH
- 5%
- Saccular Aneurysm/ Berry Aneurysm- localized dilation of a vessel wall
in which a small area
- c/c: “worst headache in my life”
- Sites:
Anterior Communicating Artery
ICA
MCA
Etiologic Classification
Grading for SAH
Etiologic Classification
C. Arteriovenous malformation (AVM)
- another congenital defect that can result in stroke.
- AVM is characterized by a tortuous tangle of arteries and veins with
agenesis of an interposing capillary system.
- The abnormal vessels undergo progressive dilation with age and
eventually bleed in about 50% of cases
Triad: Migraine, Seizure, Hemorrhage
Circle of Willis
• Location: base of the brain
• Has 9 major components
Right Hemisphere Stroke vs. Left Hemisphere Stroke
Right Hemisphere Stroke vs. Left Hemisphere Stroke
 ACA/MCA/PCA Syndromes
ACA MCA PCA

LE>UE UE>LE Visual Impairments

Astasia Aphasia Visual agnosia
Abasia Unilateral neglect Color agnosia
Abulia Apraxia (dyschromatopsia)
(+) palmar grasp Astereognosis Memory
(+) Gegenhalten * Lenticulostriate impairment
(+) Urinary artery/ artery of Alexia
Incontinence Apoplexy Thalamic pain
* Artery of Heubner syndrome
Vascular Syndrome
• Anterior Cerebral Artery Syndrome
- the anterior cerebral artery (ACA) is the first and smaller of two
terminal branches of the internal carotid artery.
- It supplies the medial aspect of the cerebral hemisphere (frontal and
parietal lobes) and subcortical structures, including the basal ganglia
(anterior internal capsule, inferior caudate nucleus), anterior fornix,
and anterior four-fifths of the corpus callosum
Anterior Cerebral Artery Syndrome
Vascular Syndrome
• Middle Cerebral Artery Syndrome
- the middle cerebral artery (MCA) is the second of the two main
branches of the internal carotid artery and supplies the entire lateral
aspect of the cerebral hemisphere (frontal, temporal, and parietal
lobes) and subcortical structures, including the internal capsule
(posterior portion), corona radiata, globus pallidus (outer part), most of
the caudate nucleus, and the putamen
Middle Cerebral Artery Syndrome
Vascular Syndrome
• Internal Carotid Artery Syndrome
- Occlusion of the internal carotid artery (ICA) typically produces
massive infarction in the region of the brain supplied by the middle
cerebral artery
- The ICA supplies both the MCA and the ACA
Vascular Syndrome
• Posterior Cerebral Artery Syndrome
- the two posterior cerebral arteries (PCAs) arise as terminal branches
of the basilar artery and each supplies the corresponding occipital lobe
and medial and inferior temporal lobe. It also supplies the upper
brainstem, midbrain, and posterior diencephalon, including most of the
thalamus
Posterior Cerebral Artery Syndrome
Posterior Cerebral Artery Syndrome
Lacunar Stroke
• Lacunar strokes are caused by small vessel disease deep in the
cerebral white matter (penetrating artery disease). They are strongly
associated with hypertensive hemorrhage and diabetic microvascular
disease
Lacunar Stroke
• Pure motor lacunar stroke
-posterior limb of the internal capsule
-pons
-pyramids
• Pure sensory lacunar stroke
- ventrolateral thalamus
- thalamocortical projections
Lacunar Stroke
• dysarthria/clumsy hand syndrome
- base of the pons
- genu of anterior limb
- internal capsule
• ataxic hemiparesis
- pons
- genu of internal capsule
- corona radiata
- cerebellum
Lacunar Stroke
• sensory/motor stroke
- involving the junction of the internal capsule and thalamus
• dystonia/involuntary movements
- choreoathetosis with lacunar infarction of the putamen or globus
pallidus
-hemiballismus with involvement of the subthalamic nucleus
Vascular Syndrome
• Vertebrobasilar Artery Syndrome
- the vertebral arteries arise from the subclavian arteries and travel
into the brain along the medulla where they merge at the inferior
border of the pons to form the basilar artery.
Vascular Syndrome
• Vertebrobasilar Artery Syndrome
-The vertebral arteries supply the cerebellum (via posterior inferior
cerebellar arteries) and the medulla (via the medullary arteries).
- The basilar artery supplies the pons (via pontine arteries), the internal
ear (via labyrinthine arteries), and the cerebellum (via the anterior
inferior and superior cerebellar arteries).
- The basilar artery then terminates at the upper border of the pons
giving rise to the two posterior arteries
Vascular Syndrome
• Vertebrobasilar Artery Syndrome
- Locked-in syndrome (LIS) occurs with basilar artery thrombosis and
bilateral infarction of the ventral pons. LIS is a catastrophic event with
sudden onset. Patients develop acute hemiparesis rapidly progressing
to tetraplegia and lower bulbar paralysis (CNs V through XII are
involved)
VBA Syndrome
• Weber- Medial Basal Midbrain
• Benedikt- Tegmentum of the midbrain
• Locked in- Bilateral basal pons
• Millard Gubler- Lateral Pons
• Wallenburg- Lateral medulla
Neurological Complications and Associated Conditions

• Altered Consciousness
- Consciousness refers to a state of arousal accompanied by awareness
of one’s environment
- Lethargy refers to altered consciousness in which a person’s level of
arousal is diminished. The lethargic patient appears drowsy but when
questioned can open the eyes and respond briefly. The patient easily
falls asleep if not continually stimulated and does not fully appreciate
the environment.
Neurological Complications and Associated Conditions

- Obtunded state refers to diminished arousal and awareness. The

obtunded patient is difficult to arouse from sleeping and once aroused,
appears confused. Attempts to interact with the patient are generally
nonproductive. The patient responds slowly and demonstrates little
interest in or awareness of the environment
Neurological Complications and Associated Conditions

- Stupor refers to a state of altered mental status and responsiveness

to one’s environment. The patient can be aroused only with vigorous
or unpleasant stimuli (e.g., painful stimuli such as flexion of the great
toe, sharp pressure or pinch, or rolling a pencil across the nail bed)
- The unconscious patient is said to be in a coma and cannot be
aroused. There are no sleep-wake cycles.
Neurological Complications and Associated Conditions

• Dysphagia
- inability to swallow or difficulty in swallowing, occurs in about 51% of
patients with stroke
- Cranial nerve involvement results in swallowing dysfunction of the
oral stage (CN V [trigeminal], CN VII [facial]), the pharyngeal stage (CN
IX [glossopharyngeal], CN X [vagus], and CN XI [accessory]), or oral and
pharyngeal (CN XII [hypoglossal])
Neurological Complications and Associated Conditions

• Cognitive Dysfunction
- may be present with lesions involving the cortex and includes
impairments in alertness, attention, orientation, memory, and
executive functions.
Neurological Complications and Associated Conditions

• Altered Emotional Status

- Lesions of the brain affecting the frontal lobe, hypothalamus, and
limbic system can produce a number of emotional changes
- The patient with stroke may demonstrate pseudobulbar affect (PBA),
also known as emotional lability or emotional dysregulation
syndrome. PBA occurs in about 18% of cases.
Neurological Complications and Associated Conditions

• Aphasia
- general term used to describe an acquired communication disorder
caused by brain damage and is characterized by an impairment of
language comprehension, formulation, and use.
Aphasia Naming Comprehension Fluency Repetition Reading Writing
Comprehension
Anomia
Conduction
Transcortical
motor
Brocha's
Transcortical
Sensory
Wernicke's
Isolation
Global
Neurological Complications and Associated Conditions

• Tone
Flaccidity- (hypotonicity) is present immediately after stroke and is
due primarily to the effects of cerebral shock. It is generally short-lived,
lasting a few days or week
Spasticity- (hypertonicity) emerges in about 90% of cases and occurs
on the side of the body opposite the lesion
Modified Ashworth Scale
Neurological Complications and Associated Conditions

• Associated Reflexes
(Reading Assignment)
Neurological Complications and Associated Conditions

• Voluntary Movements
- Abnormal and highly stereotyped obligatory synergies emerge with
spasticity following stroke
Neurological Complications and Associated Conditions
Cerebrovascular Imaging
• Computed Tomography- the most commonly used and readily
available neuroimaging technique. CT resolution allows identification
of large arteries and veins and venous sinuses. It demonstratespoor
sensitivity for detecting small infarcts.
• MRI
• MRA
 Brunnstrom Stages of Recovery
I. Flaccid
II. Spasticity begins to appear
III. Peak of Spasticity
IV. Spasticity begins to decline
V. Spasticity continues to decline
VI. Disappearance of spasticity
VII. Normal
Recovery and Outcomes
• Functional mobility skills are impaired following stroke and vary
considerably from individual to individual. During the acute stroke
phase, 70% to 80% of patients demonstrate mobility problems in
ambulation whereas 6 months to 1 year later the figures are
reversed, with only 20% of patients needing help to walk
independently
Recovery and Outcomes
• Basic ADL skills such as feeding, bathing, dressing, and toileting are
also compromised during acute stroke, with 67% to 88% of patients
demonstrating partial or complete dependence
Recovery and Outcomes
• Patients who receive inpatient stroke rehabilitation (skilled
occupational, physical, and speech therapy) demonstrate improved
motor recovery, functional status, and quality of life at discharge.
Recovery and Outcomes
• Effective rehabilitation should take advantage of the brain’s capacity
for repair and recovery. Rehabilitation interventions seek to promote
recovery and independence through neurofacilitation, functional, and
compensatory training strategies.
Recovery and Outcomes
• Interventions also focus on the prevention of secondary impairments.
The utilization of effective motor learning strategies with task
oriented training for real-life environments is critical for the
successful attainment of functional outcomes